These teachings relate generally to imaging modalities based on the ability of imaging technologies to detect wave-induced tissue deformation.
Some cells, referred to as excitable cells, can reverse their resting membrane potential from negative values to slightly positive values. This rapid change in membrane potential is referred to as an action potential. Typically, the action potential is the result of a rapid change in membrane permeability to certain ions. Nerve cells and muscle cells are excitable cells. Heart muscle cells are excitable cells and their action potential is referred to as cardiac action potential (or simply as action potential).
Current technology does not allow us to see action potential propagation deep within the walls of the heart. This deficiency has a number of consequences. In the clinical setting, diagnostics such as the electrocardiogram (ECG) or electrophysiology (EP) studies are relied on to provide information about the heart's electrical state. While these tests do certainly yield a wealth of valuable information, they often do not provide a fundamental understanding of the dynamics underlying the patient's cardiac rhythm. For example, the field of cardiology is currently moving away from EP studies as a diagnostic for determining whether to implant an implantable cardioverter defibrillator (ICD), relying instead on the ejection fraction, paradoxically a mechanical rather than electrical measure, as the basis for the decision. This suggests that an improved diagnostic for assessing the patient's rhythm dynamics is needed. At the research level, this lack of a deep, panoramic view of action potential activity means that it can not be said with certainty that ventricular fibrillation (VF) is caused by multiple reentrant action potential waves, although of course it is strongly suspected. Even if VF is a manifestation of multiple waves, the nature of the dynamics of these waves remains controversial, with their induction and maintenance being attributed to either tissue heterogeneity or steep electrical restitution, and their spatial patterning thought to be composed of either several rotating waves on equal dynamical footing, or one dominant “mother rotor” wave driving fibrillatory conduction. The lack of clarity on these issues has greatly complicated the development of effective therapies for the prevention and treatment of several types of tachyarrhythmias, including VF.
This bewildering landscape of theoretical wave propagation patterns and the mechanisms for their initiation and maintenance are what have led researchers to develop tools that might be used to actually see what patterns exist during VF and other rapid, abnormal rhythms. Rudy et al. have developed an impressive, noninvasive method called ECGi to track action potential propagation on the epicardium using hundreds of electrodes situated on the body surface. This method does not as yet provide transmural information, however. Other approaches, such as the use of plunge electrodes, transillumination, and optical tomography can provide a 3D representation of the electrical activity in the heart. Plunge electrodes and transillumination can also capture the complex electrical dynamics of scroll waves in reentry. The spatial resolution of the plunge electrode method is, however, relatively low; furthermore, it is likely that the presence of these electrodes creates electrical heterogeneities that strongly modify the patterns of propagation. Both transillumination and optical tomography techniques have some light penetration problems, thus potentially making them difficult to apply to thicker myocardial walls such as those found in canine or human ventricles. Additionally, optical tomography cannot be applied in-vivo.